A population based screening of abdominal aortic aneurysms (AAA)

Eur J Vasc Surg 5, 53-57 (1991)

A Population Based Screening of Abdominal Aortic Aneurysms (AAA)* Henrik Bengtsson, 1 David Bergqvist, 2 0 l l e Ekberg 3 and Lars Janzon 4

Departments of l Surgery, 2 Radiology and 3Community Health Sciences, 4Lund University, Malta6 General Hospital, Malm6, Sweden

The prevalence of abdominal aortic aneurysm (AAA) in a defined population of elderly men and its correlation to some risk factors were studied in the population cohort "men born in 1914from Malm6". A total of 499 were invited to attend and 375 (75 %) did so. The aorta could be visualised with ultrasound in 364 patients, 39 (10.7%) of whom had aneurysmaI changes. The presence of an AAA was related to thefindings at a general health examination undertaken 5 years previously. Tobaccoand alcohol consumption, impaired lung function and a history of angina pectoris were related to the presence o/an AAA. No relationship was found between an A A A and hypertension, hyperlipidaemia or hyperglycaemia. A decreased tissue elasticity as a common denominator for the lung function impairment and development of A A A is discussed. Key Words: Abdominal aortic aneurysm; Screening.

Introduction

Materials and Methods

The prevalence of an abdominal aortic a n e u r y s m (AAA) a n d its natural course are relatively uncertain. A majority of the studies, which have e x a m i n e d the e p i d e m i o l o g y of AAA are based on selected g r o u p s of individuals w h o are often poorly defined in terms of age a n d sex 1 a n d risk factors have usually b e e n based o n selected g r o u p s with a retrospective s t u d y design. The relationship b e t w e e n atherosclerosis a n d AAA is controversial. The population s t u d y " m e n b o r n in 1914 from Malm6", Sweden, is a unique prospective investigation designed to assess the cardiovascular morbidity a n d mortality and their major determinations in those elderly men. The aim of the p r e s e n t part of the p r o g r a m m e was to d e t e r m i n e the prevalence of ultrasonographicalty detected AAA and to s t u d y the relationship to k n o w n risk factors for cardiovascular disease.

The city of Malm6 is situated in the south of S w e d e n a n d had a p o p u l a t i o n of about 230 000 inhabitants in 1988. The cohort in this s t u d y includes all m e n born in e v e n m o n t h s in 1914 a n d w h o in 1982-1983 were registered as citizens of Malm6. These m e n have been invited to have various clinical, physiological, biochemical and sociological examinations over the last two decades. Those 499 w h o were living in Malm6 on the 1st October 1988 were invited for ultrasonographic examination of their abdominal aorta and a second invitation issued to those w h o did not r e s p o n d to the first one. The examination was p e r f o r m e d by one radiologist specially trained in u l t r a s o n o g r a p h y on the realtime e q u i p m e n t being used. Individuals were asked to fast for 4 h prior to the visit. The m a x i m u m transverse aortic diameter at the level of the coeliac axis and just proximal to the bifurcation was m e a s u r e d and any dilatation b e t w e e n these two sites were recorded. An a n e u r y s m of the abdominal aorta (AAA) was defined as a bulging of the intrarenal aorta or w h e n the external abdominal aorta diameter exceeded 35 mm, and the prevalence was related to findings at the health examination that these m e n were invited to in 19821983 w h e n the a t t e n d a n c e rate was approximately

* Presented at the 4th Annual Meeting of the European Society for Vascular Surgery, Rome, September 1990.

Please address all correspondence to: Henrik Bengtsson, M.D., Department of Surgery, Malm6 General Hospital, S-21401 Malm6, Sweden. 0950-821X/91/010053+05$03.00/0© 1991Grune & Stratton Ltd.

H. B e n g t s s o n et aL

54

80% .2 Because some of the m e n w h o did not a t t e n d the health examination came to the u l t r a s o u n d examination, some of the parameters previously r e c o r d e d w e r e not available for comparison in all of them. The prevalence of AAA was related to cardiovascular risk factors. The smoking habits were based on an interview using a structured questionnaire, and individuals were classified as non-smokers, ex-smokers (stopped smoking m o r e than I m o n t h before the interview) or smokers. The smoking duration in years and tobacco c o n s u m p t i o n per w e e k were estimated. H e a v y smokers w e r e defined as those with an estim a t e d tobacco c o n s u m p t i o n of 25 cigarettes per d a y or more. The average alcohol c o n s u m p t i o n d u r i n g the p r e c e d i n g year was estimated in grams of alcohol per w e e k using a structured questionnaire. 3 Standard laboratory m e t h o d s were used to determine s e r u m creatinine, fasting blood glucose, fasting plasma cholesterol and triglycerides. Body w e i g h t was m e a s u r e d to the nearest 0.5 kg, height to the nearest centimetre a n d b o d y mass index (BMI) c o m p u t e d as weight/ length 2 (kg/m2). Systolic and diastolic blood pressure was m e a s u r e d with a m e r c u r y m a n o m e t e r after 15 min sitting at rest and the pressure recorded to the nearest 5 m m H g . Arterial h y p e r t e n s i o n was defined as a diastolic pressure equal to or more than 105 m m H g and/or t r e a t m e n t for h y p e r t e n s i o n . L u n g function tests were p e r f o r m e d using conventional s p i r o m e t r y (Bernstein type spirometer) and a multiple breath nitrogen w a s h o u t test. 4'5 Vital capacity (VC), forced expiratory v o l u m e in one second (FEV1), total lung capacity (TLC), residual v o l u m e (RV), RV in per cent of TLC (RV%) and w a s h o u t v o l u m e (WOV) were calculated. Closing v o l u m e (CV) a n d slope index (SI) were m e a s u r e d using the Xenon 133 technique, 6 and CV a n d SI as a percentage of vital capacity (CV% and SI%) were also calculated. The degree of arteriosclerotic leg disease was assessed b y the ankle brachial pressure ratio and a ratio of less than 0.9 considered as abnormal. The presence of angina pectoris was established using the Rose questionnaire 7 and a history of myocardial infarction validated t h r o u g h the Malm6 city myocardial infarction register. The presence of internal carotid artery stenosis was established b y Doppler flow m e a s u r e m e n t s , frequencies above 3.0 kHz being u s e d to define carotid artery disease causing a stenosis of more than 30% .9

with a n d without AAA, and p value <0.05 was considered as statistically significant.

Results

According to the p o p u l a t i o n register at the time of this study, 499 m e n fulfilling the inclusion criteria were still alive. After two invitations a total of 375 m e n (75%) a t t e n d e d for u l t r a s o u n d examination. The aorta could not be seen in seven individuals. Of the r e m a i n d e r four already had an aortic graft, two because of AAA a n d two because of occlusive aortoiliac disease. The m e d i a n aortic diameter at the coeliac axis was 25 m m (range 17-35 mm) and at the aortic bifurcation 19 m m (range 12-60 ram). The m a x i m u m external abdominal aortic diameter a m o n g all registered cases is illustrated as a histogram (Fig. 1). An AAA with a m a x i m u m external diameter from 25 to 70 m m (median 32 mm) was f o u n d in 39 (10.7%) of m e n (95% confidence limits 7.5 % - 13.9 %). The a n e u r y s m diameters are illustrated in m o r e detail in Figure 2. There was a localised dila-

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Fig. 1. Maximum outer diameter of abdominal aorta, measured by ultrasonography, among 364 men aged 74 in Malm6, Sweden. 15

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Aneurysm size

Analyses of variance and Chi-square analyses were u s e d for c o m p a r i s o n of risk factor distributions in m e n Eur J Vasc Surg Vol 5, February 1991

Fig. 2. Maximum outer diameter of abdominal aortic aneurysms, measured by ultrasonography, in 39 men aged 74.

Abdominal Aortic Aneurysms

55

Table 1. Mean values and SD for different cardiovascular risk factors and lung function parameters in 74-year-old men with and without an abdominal aortic aneurysm

Parameter

AAA (N = 39) Mean

SD

Normal (N = 299) Mean

SD

Length (cm)

176

(± 6.5)

174

(± 6.5)

NS

Weight (kg)

77

(+ 12)

76

(+ 11)

NS

Body mass index (kg/m2)

25

(_+3.6)

25

(± 3.2)

NS

Blood pressure (mmHg) Systolic

157

(+ 23)

151

(+ 21)

NS

94

(+ 10)

92

(+ 10)

NS

Diastolic Serum lipids (mmol/1) Triglycerides Cholesterol Blood glucose (mmol/1)

1.5

(+ 0.6)

1.5

(+ 0.7)

NS

6.1

(± 1.1)

6.0

(+ 1.0)

NS

5.2

(± 1.4)

5.1

(+ 1.1)

NS

Weekly alcohol consumption (g)

131

(± 175)

86

(+ 106)

p<0.05

Weekly tobacco consumption (g)

55

(± 91)

27

(+ 51)

p<0.01

Smoking years

36

(± 19)

29

(+ 20)

p<0.05

Lung function tests VC

4.0

(+ 0.7)

4.2

(+ 0.6)

NS

FEVI.o

2.8

(+ 0.7

3.0

(± 0.6)

NS

TLC

6.8

(+ 0.9)

6.7

(± 1.0)

NS

RV

2.7

(+ 0.6)

2.5

(+ 0.7)

p<0.05

RV (%)

40

(+ 6.7)

37

(+ 6.8)

p<0.01

WOV

42

(+ 14)

35

(+ 12)

p<0.0001

CV (%)

28

(+ 7.2)

29

~ (_+ 7.3)

SI (%)

(+ 1.8)

2.8

2.0

(+ 1.2)

NS p< 0.0001

NS = not significant. Table 2. Presence of hypertension and symptomatic arteriosclerotic lesions in 74-year-old men with and without an abdominal aneurysm

Risk factors

With AAA N = 39

Without AAA N = 299

Hypertension

50%

42%

NS

Angina pectoris

28%

11%

p<0.05

Previous myocardial infarction

19%

10%

NS

Occlusive leg artery disease

12%

8%

NS

Carotid artery stenosis

22%

29°/,,

NS

NS = not significant.

tat±on in each case of A A A a n d n o m e g a - a o r t a s w e r e found. T h e s m o k i n g habits h a d p r e v i o u s l y b e e n establ i s h e d in 341 of t h o s e successfully i n v e s t i g a t e d b y u l t r a s o u n d . A m o n g t h e s e 69 (20%) h a d n e v e r s m o k e d , 161 (47%) w e r e d e f i n e d as e x - s m o k e r s a n d 111 (33%) as s m o k e r s , A A A b e i n g f o u n d in 5 (7.2%), 17 (10.6%) a n d 17 (15.3%), r e s p e c t i v e l y (NS). W h e n the m e n w e r e classified a c c o r d i n g to t h e d u r a t i o n of s m o k i n g (rangi n g f r o m z e r o to 60 years) t h o s e w i t h A A A h a d s m o k e d for a significantly l o n g e r p e r i o d (Table 1). T h e w e e k l y t o b a c c o c o n s u m p t i o n w a s also h i g h e r a m o n g m e n w i t h A A A (Table 1). Eight m e n w e r e d e f i n e d as h e a v y s m o k e r s a n d of t h e s e t h r e e h a d a n A A A . Alcohol consumption, impaired lung function a n d a h i s t o r y of a n g i n a p e c t o r i s w e r e also significantly r e l a t e d to the p r e s e n c e of A A A (Tables I a n d 2). Eur J Vasc Surg Vol 5, February 1991

56

H. Bengtsson et al.

In order to further analyse the influence of other risk factors we stratified the material on the basis of smoking habits. Among the non-smokers, none of the factors studied at the health examination 1982-1983 were related to AAA. Among smokers however there was a significant relationship to tests showing impaired lung function and a history of angina pectoris but not to alcohol consumption.

Discussion

Because an aneurysm develops from a normal aorta and its size depends on when it is diagnosed, the definition of AAA is controversial. 9 As ultrasonograp h y and CT have made it possible to find very small aneurysms we have chosen to include minimal aneurysmal changes in the infrarenal aorta in this study. The attendance rate in our investigation was 75%, which compares favourably with other population based aneurysm screening studies. 1°-12 A low participation rate may seriOusly invalidate the result due to the selection bias caused by non-responders in whom the prevalence of alcoholism and various chronic disorders such as atherosclerosis and cancer are higher. 2 As a result one can assume that the observed prevalence of AAA in this study is, if anything, an underestimate. Three other prevalence studies of AAA have previously been published. 10-12 In two of these an AAA with a diameter of 4 cm or more was found in 2.4 (10) and 1.5% (12) compared with 3.3% in our study. The higher prevalence in our study may be explained by the older age of the participants and by the fact that it was restricted to men. 1,13 Although the baseline parameters used in this study were registered 5 years before the ultrasonographic examination, the documented slow expansion of small aneurysms 14 makes is probable that a large proportion of the aneurysmal changes were already present at that time, making it reasonable to consider the observed associations as valid in relation to AAA. The relationship between AAA and a history of smoking is strongly supported by an autopsy study, is aneurysms being eight times more common among smokers. In our study there was an association between both the duration of smoking and the tobacco consumption per week and the presence of AAA suggesting a cumulative effect. Hypertension as a risk factor for the development of AAA has been suggested on theoretical grounds as well as from crosssectional population studies. 16-19 Surprisingly we found no such relationship which might be explained Eur J VascSurgVol5, February1991

on the grounds of selection bias, i.e. individuals with a higher blood pressure might already be dead from cardiovascular disease. However, it might also be that there is no association between AAA and hypertension. Of the various manifestations of occlusive arterial disease such as angina pectoris, a history of myocardial infarction, reduced ankle-brachial pressure index and internal carotid artery stenosis only angina pectoris correlated with AAA. This is in agreement with the results of an autopsy study where coronary artery disease was found to be related to AAA. 2° In contrast to our observations, Collin found a relationship between AAA and signs or symptoms of peripheral occlusive disease, 1° which could be due to differences in study design. Because both the manifestations of arteriosclerotic disease and AAA are common in elderly people it is difficult to study potential causal relationships and the problem can only be solved in properly designed prospective studies. The relationship between a high alcohol consumption and AAA disappeared when the study group was stratified with regard to smoking habits, which suggests that the relationship to alcohol may be spurious. The relative residual volume (RV%), washout volume (WOV) and relative slope index (SI%) were all very significantly related to the presence of AAA. These tests are interestingly all sensitive indicators of the elastic function of the lung, 7 increased values meaning a decrease in elasticity. Our results suggest that smokers with lung function tests indicating low elasticity are high risk individuals for AAA. Evidence is now emerging that there is increased elastolytic activity and a decrease in the amount of elastin found in the arterial media of AAAs. 21"22 Cronenwett et al. found obstructive pulmonary disease to be one of three independent risk factors for AAA rupture. 23 These observations would suggest a decreased elasticity in various tissues in individuals with AAA, but whether this is due to an inborn defect or a common tissue response in certain individuals to factors such as smoking remains to be clarified.

Acknowledgements The study was supported by grants from the Swedish Medical Research Council00759 (SMRC),the SwedishNationalAssociation against Heart and Chest Diseases and Facultyof Medicine, Lund University.

Abdominal Aortic Aneurysms

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12 O'KELLY TJ, HEATHER BP. General practice-based population screening for abdominal aortic aneurysms: a pilot study. Br ] Surg 1989; 76: 479-480. 13 BENGTSSONH, BERQWSTD, STERNBYNH. Increasing prevalence of abdominal aortic aneurysms - an autopsy-based study (in press). 14 HEATHER BP, COLLIN J, WALTON J. Incremental growth rates of abdominal aortic aneurysms less than 4.0 cm diameter. From John Radcliffe Hospital, Oxford, England (submitted). 15 AUERBACH O, GARFINKEL L. Atherosclerosis and aneurysm of aorta in relation to smoking habits and age. Chest 1980; 78: 805. 16 ALLEN PIM. Screening for abdominal aortic aneurysm. Biomed Pharmacother 1988; 42: 451-454. 17 LEDERLE FA, WALKER JM, REINKE DB. Selective screening for abdominal aortic aneurysms with physical examination and ultrasound. Arch Intern Med 1988; 148: 1753-1756. 18 TWOME¥ A, TWOMEY E, WILKINS RA, LEWIS JD. Unrecognised aneurysmal disease in male hypertensive patients. Inter Angio 1986; 5: 269-273. 19 THURMOND AS, SEMLERHJ. Abdominal aortic aneurysm:incidence in a population at risk. J Cardiovasc Surg 1986; 27: 457-460. 20 BERQVISTD, BENGTSSONH, STERNBYNH. Associated atherosclerotic manifestations. In GREENHALGH RIV[, MANNICKJA, POWELL JT, eds. The Cause and Management of Aneurysms. London: WB Saunders Company, 1990. 21 POWELL J, GREENHALGH R/'VI. Cellular, enzymatic, and genetic factors in the pathogenesis of abdominal aortic aneurysms. J Vasc Surg 1989; 9: 297-304. 22 COHENJR, MANDELLC, CHANGJB, WISE L. Elastin metabolism of the infrarenal aorta. J Vasc Surg 1988; 7: 210-214. 23 CRONENWETTJL, MuRPHY TF, ZELENOCKGB, et al. Actuarial analysis of variables associated with rupture of small abdominal aortic aneurysms. Surgery 1985; 98: 472-482.

Accepted 17 October 1990

Eur J Vasc Surg Vol 5, February 1991